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Frank Block - One of the best experts on this subject based on the ideXlab platform.
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Gabapentin therapy for pain
Der Nervenarzt, 2001Co-Authors: Frank BlockAbstract:Gabapentin, which has been approved for add-on therapy of focal seizures, is increasingly used for treatment of neuropathic pain. Its analgesic effect is supposed to be due to reduction of glutamatergic transmission, improvement of GABAergic transmission and to binding to voltage-dependent calcium channels. Experimental studies demonstrated an ameliorating effect of gabapentin on neuropathic pain. Placebo-controlled studies revealed an efficacy of gabapentin against pain in diabetic neuropathy and postherpetic Neuralgia and in prophylaxis of migraine. Case reports show an analgesic effect of gabapentin in Trigeminus Neuralgia and in reflex sympathetic dystrophy. The main adverse events are dizziness, ataxia and somnolence. Controlled studies, which compare the efficacy of gabapentin with that of the respective reference drug, are needed to evaluate its importance in treatment of pain.
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Gabapentin zur Schmerztherapie
Der Nervenarzt, 2001Co-Authors: Frank BlockAbstract:Gabapentin, which has been approved for add-on therapy of focal seizures, is increasingly used for treatment of neuropathic pain. Its analgesic effect is supposed to be due to reduction of glutamatergic transmission, improvement of GABAergic transmission and to binding to voltage-dependent calcium channels. Experimental studies demonstrated an ameliorating effect of gabapentin on neuropathic pain. Placebo-controlled studies revealed an efficacy of gabapentin against pain in diabetic neuropathy and postherpetic Neuralgia and in prophylaxis of migraine. Case reports show an analgesic effect of gabapentin in Trigeminus Neuralgia and in reflex sympathetic dystrophy. The main adverse events are dizziness, ataxia and somnolence. Controlled studies, which compare the efficacy of gabapentin with that of the respective reference drug, are needed to evaluate its importance in treatment of pain. Gabapentin, welches seit einigen Jahren als Zusatzmedikament für die Therapie fokaler Anfälle zugelassen ist, wird vermehrt in der Behandlung neuropathischer Schmerzen eingesetzt. Eine Verringerung glutamaterger Transmission, eine Verstärkung der GABAergen Transmission und eine Bindung an spannungsabhängige Kalziumkanäle werden als Mechanismen der schmerzlindernden Wirkung von Gabapentin diskutiert. Experimentelle Untersuchungen belegen die Wirkung von Gabapentin beim neuropathischen Schmerz. Der Wirkort liegt vermutlich im Dorsalhorn des Rückenmarkes. Für die diabetische Polyneuropathie, die postherpetische Neuralgie und die Migräneprophylaxe weisen plazebokontrollierte Studien eine Wirksamkeit von Gabapentin nach. Für die Trigeminusneuralgie und die sympathische Reflexdystrophie wird eine schmerzlindernde Wirkung bisher nur durch Fallberichte gestützt. Die effektive Dosis liegt zwischen 1200 und 3600 mg/Tag. Als häufigste Nebenwirkungen werden Schwindel, Ataxie und Müdigkeit genannt. Um den endgültigen Stellenwert von Gabapentin in der Schmerztherapie abzuschätzen, muss auf die Ergebnisse kontrollierter Studien gewartet werden, die Gabapentin mit der jeweiligen Referenzsubstanz vergleichen.
Maija Haanpää - One of the best experts on this subject based on the ideXlab platform.
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Trigeminal Neuralgia and other facial pain
2000Co-Authors: Maija HaanpääAbstract:Trigeminal Neuralgia and other facial pain Trigeminal NeuralgiaEssentialsTrigeminal Neuralgia is characterized by paroxysms of intense pain resembling electrical shocks on the other half of the face in the area of one or two of the branches of the trigeminal nerve.Idiopathic trigeminal Neuralgia is not caused by any other disease and there are no findings in imaging investigations.First line drug is carbamazepine.In some patients, the symptom is relieved within a period of a few months, and thus the medication can be gradually reduced after achieving treatment response.Symptoms Between the attacks the pain is totally absent (remission phase), and in the active phase it may be provoked typically by touching certain areas of the face (trigger zones) or by eating. A new pain episode can be provoked after a refractory period that lasts from some seconds to some minutes. The pain comes in very short attacks of shooting pain or ”pins-and-needles” sensations. Additionally, continuous pain may occur. In the idiopathic trigeminal Neuralgia, there are no permanent neurological deficiency symptoms. When at its worst, trigeminal Neuralgia may prevent the patient from washing the face or brush the teeth and make her/him unable to speak or even eat and drink. Causes and diagnosis In idiopathic trigeminal Neuralgia there is no underlying disease or vascular compression upon the trigeminal nerve causing the condition. About 10% of the patients belong to this group. In the majority of patients the symptoms are explained by vascular compression upon the trigeminal nerve in the brain stem. Symptomatic trigeminal Neuralgia has similar symptoms as the idiopathic form but it is caused by another disease, e.g. MS or a brain stem tumour. Classification of trigeminal NeuralgiaPotential trigeminal Neuralgia: the patient has a unilateral pain resembling electrical shocks, limited to the area of a branch of the trigeminal nerve.Clinically confirmed trigeminal Neuralgia: the patient has a unilateral pain resembling electrical shocks, limited to the area of a branch of the trigeminal nerve, and the pain may be provoked by a typical stimulus (e.g. breath of wind, touch, eating, movement of the muscles of facial expression).Idiopathic trigeminal Neuralgia with confirmed aetiology: in addition to the criteria in item 2, vascular compression upon the trigeminal nerve is detected by MRI, associated with morphological changes in the trigeminal nerve root (requires 3D reconstruction technique).Secondary trigeminal Neuralgia: in addition to the criteria in item 2, an MS plaque or a tumour causing trigeminal Neuralgia is detected by MRI.Treatment The drug of choice is carbamazepine which is dosed according to response. Oxcarbazepine is an alternative and may be tried especially if carbamazepine causes adverse effects (fatigue, dizziness) or when there is a need to avoid the interactions of carbamazepine with other drugs. It is a derivative of carbamazepine but better tolerated. Oxcarbazepine is as effective as carbamazepine in trigeminal Neuralgia. The initial dose for carbamazepine is 100 mg × 2 and for oxcarbazepine 150 mg × 2. The dose can be increased up to 1 200 mg/24h with carbamazepine and up to 1 800 mg/24h with oxcarbazepine. In the beginning follow-up of blood cell counts and liver function tests is recommended. Carbamazepine concentration can be measured if there are signs of overdose (dizziness, tiredness, diplopia or nystagmus).Because trigeminal Neuralgia has a tendency for spontaneous remission, a trial may be made to taper off the medication gradually after a few months.If trigeminal Neuralgia remains refractory to carbamazepine or oxcarbazepine, the patient is referred to specialized care for therapeutic assessment (e.g. department of neurology or neurosurgery). The most commonly used neurosurgical treatment modalities include coagulation of the trigeminal ganglion and microvascular decompression, i.e. microsurgical release of the nerve compression caused by a small nearby artery . Other drugs may be tried if carbamazepine or oxcarbazepine are ineffective or not tolerated and the patient is not willing to undergo neurosurgical treatment. There is evidence on the effectiveness of lamotrigine as an add-on drug to carbamazepine (note: risk for skin rash when increasing thedosage). Also baclofen has been shown to have effect in trigeminal Neuralgia. Dosage may be increased up to 80 mg/24h if needed. Phenytoin, clonazepam, valproic acid, gabapentine or pregabalin may be tried as secondary alternatives, but there is no evidence of their efficacy. Intravenous phosphenytoin may be tried for severe exacerbations even if its efficacy has not been proven in randomized controlled trials. After the infusion the medication is continued orally aiming at an effective yet tolerable dosage. When one drug is not enough, a combination of several drugs with different action mechanisms may be tried in patients who are not willing to undergo neurosurgical treatment.Therapy with botulinum toxin A (25–100 units) may be tried in Trigeminus Neuralgia refractory to the first-line drugs. Other facial pains Other neuropathic pain in the facial area In another type of facial neuropathic pain, a damage to a branch of the trigeminal nerve has led to a neuropathic pain state. The pain is usually long-term steady aching or burning, and the patient may in addition experience pains resembling electrical shocks.The most common causes of facial neuropathic pain include facial injuries, sequelae of surgical interventions (e.g supraorbital nerve injury in association with Beck's trepanation of the frontal sinus) and postherpetic Neuralgia . The pain may also emerge after a disturbance of the cerebral circulation (so-called central post stroke pain). In these patients, the pain and the sensory disturbance do not necessarily limit to the facial area. Careful sensory testing of the face or neurophysiological investigations will reveal abnormal findings.If a patient is diagnosed with facial neuropathic pain of unclear origin, he/she is referred to a neurologist for further investigations. Other facial pain Acute facial pain is most commonly caused by sinusitis or by factors of dental origin. The aetiology may also be a disturbance of the masticatory system, or the pain may be referred from the anterior neck (e.g. thyroiditis) or from the back of the neck (e.g. tension neck).So-called atypical facial pain, also called persistent (or chronic) idiopathic facial pain (PIFP), is a much more common type of prolonged facial pain than trigeminal Neuralgia. The pain is usually constant and dull. It is not restricted to one half of the face and is also otherwise independent of dermatomal borders. The pain may be triggered by an intervention directed at the paranasal sinuses or at the teeth (not, however, being a complication of the intervention), infection or stress.PIFP most commonly occurs in middle-aged women. The patients are often subjected to psychosocial stress. Clinical examination of a patient with facial pain includes teeth, masticatory muscles, temporomandibular joints, cervical spine and muscles of the neck and shoulders. It may also be advisable to examine the ears, nose and throat as well as the eyes and the anterior neck.If neuropathic pain is suspected, a neurological examination is important especially concerning the cranial nerves.A patient with severe or progressive facial pain is referred for further investigations to specialized care either to the department of oral diseases, neurology or ENT or to a special pain clinic, according to the local practice guidelines. See also cluster headache . TreatmentOther neuropathic pain in the facial area The treatment of other neuropathic pains in the facial area follows the same conventional principles as the treatment of any neuropathic pain .First-line drugs for neuropathic pain are gabapentin, pregabalin, tricyclic antidepressants and antidepressants of the SNRI group.Persistent idiopathic facial pain (PIFP)PIFP is treated primarily with antidepressants. Tricyclic antidepressants are used in small dosages, venlafaxine in similar dosage as in the treatment of depression.Other facial painTreatment is determined by the cause of the pain. If the pain is suspected to originate from dental occlusion or from the teeth, the patient is referred to a dentist for assessment. Related resources Cochrane reviews Literature Morra ME, Elgebaly A, Elmaraezy A et al. Therapeutic efficacy and safety of Botulinum Toxin A Therapy in Trigeminal Neuralgia: a systematic review and meta-analysis of randomized controlled trials. J Headache Pain 2016;17(1):63. Cruccu G, Finnerup NB, Jensen TS et al. Trigeminal Neuralgia: New classification and diagnostic grading for practice and research. Neurology 2016;87(2):220-8. Zakrzewska JM, Linskey ME. Trigeminal Neuralgia. BMJ 2014;348():g474. Headache Classification Subcommittee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia 2013; 33: 629–808.Gronseth G, Cruccu G, Alksne J et al. Practice parameter: the diagnostic evaluation and treatment of trigeminal Neuralgia (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology and the European Federation of Neurological Societies. Neurology 2008;71(15):1183-90.
Institut Fuer Luft- Und Kaeltetechnik Gmbh, Dresden Fachbereich Kryotechnik - One of the best experts on this subject based on the ideXlab platform.
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Entwicklung und klinische Erprobung von Spezialsonden fuer die Kryomdeizin. Eine vakuumisolierte Kryosonde zur Trigeminus-Schmerzausschaltung Abschlussbericht
1993Co-Authors: Herzog R., Spoerl, Akademie E. Dresden, Eckelt U., Krantz H., Schumann B., Binneberg A., Institut Fuer Luft- Und Kaeltetechnik Gmbh, Dresden Fachbereich KryotechnikAbstract:To the not surgical treatment the Trigeminus-Neuralgia was developed a novel cryoprobe. This probe is composed of a small tube-system, which is joined with a reservoir filled with liquid nitrogen. On the construction, lab-tests and over first successful clinical applications is reported. (orig.)Available from TIB Hannover: F95B90+a / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEBundesministerium fuer Forschung und Technologie (BMFT), Bonn (Germany)DEGerman
M. Bodosi - One of the best experts on this subject based on the ideXlab platform.
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Trigeminus Neuralgia kezelése microvascularis dekompresszióval.
Orvosi hetilap, 1997Co-Authors: Kuncz A, Zoltán Mencser, Erika Vörös, M. BodosiAbstract:The experience with a series of 28 posterior fossa exploration and microvascular decompression for trigeminal Neuralgia is presented. All the patients were treated with carbamazepine previously and some of them were operated on by destructive methods. The diagnostic work-up consisted of an accurate history, CT or MRI in all cases, and recently (in 17 cases) the vascular compression of the trigeminal nerve was demonstrated directly by MR angiography in the plane of the trigeminal nerve. Microvascular decompression was performed through a suboccipital retromastoid craniotomy. At the operations 21 arterial, 4 venous, 2 combined (arterial + venous) and 1 arachnoid band compression were found. The mean follow up was 30 months. Immediate pain relief was achieved in all cases but one, and there were two recurrences 6 and 12 months later (both of them were venous compression), which have been controllable medically since then. There were 3 permanent hypaesthesia of the face (one of them loss of corneal reflex), 2 hypacusis, 1 cerebrospinal fluid leakage and 1 cerebellar edema as complications. Microvascular decompression is a safe and effective treatment for trigeminal Neuralgia and advised if the medical treatment is failed, the patient suitable for general anaesthesia, and there is the evidence of vascular compression of trigeminal nerve on MR angiography.
O. Dagtekin - One of the best experts on this subject based on the ideXlab platform.
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Chili for therapy of Trigeminus Neuralgia: a case report
Schmerz (Berlin Germany), 2012Co-Authors: J. Loeser, B. Pilgram, O. DagtekinAbstract:We report the case of a 39-year-old female patient who suffered from trigeminal Neuralgia of the left lingual nerve for 6 years. The previous therapy according to the guidelines including a Jannetta operation was unsuccessful. Only after beginning with daily mastication and consumption of very hot chilli peppers has the patient become reliably pain-free.
